S. pneumoniae is a gram-positive bacterial organism that colonizes the upper respiratory tract and causes life-threatening diseases such as pneumonia, bacteremia and meningitis throughout the world. Currently, more than one million children die each year from pneumococcal-associated diseases.
S. pneumoniae colonizes the nasopharynx asymptomatically, leading to a clinically-silent carriage state. Carriage is most prevalent in children and about 70-80% of children attending day care centers carry S. pneumoniae at any given time. In adults, the carriage rate may vary according to environmental conditions. The pathogenic mechanisms that convert this benign state of carriage into clinical disease are unknown. It is generally assumed, however, that in common with other bacterial species, development of the carriage state is dependent on recognition of host cells by S. pneumoniae and attachment thereto. It is also suspected that either the appearance of a new strain, unfamiliar to the immune system, or activation of the immune system, with another viral or bacterial pathogen, enables the invasion and spread of the bacteria into sterile tissues thereby converting the benign carriage state into a life-threatening or potentially life-threatening clinical disease.
Following attachment, the bacteria may invade the cells and tissues, thereby leading to the aforementioned disease states associated with S. pneumoniae. Bacterial attachment involves interaction between one or more bacterial surface proteins, known as adhesins, and one or more host cell receptors. By means of blocking the recognition and attachment stage it may be possible to prevent the carriage stage and hence avert the development of the abovementioned disease states. Identification of bacterial adhesins involved in attachment to host mucosal layer are of prime interest in understanding the molecular basis of bacterial interaction with the host.
Currently, there is growing resistance of S. pneumoniae to antibiotics. In addition, the currently available vaccines offer only limited protection against infection with this organism. Consequently, an urgent need exists for clinically-safe and efficacious methods of preventing the adhesion of S. pneumoniae to host cells.